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Mus musculus
9 Downloadable Samples
Description
We have previously shown that adenoviral expression of peroxisome proliferator-activated receptors (PPARs) leads to rapid establishment of transcriptionally active complexes and activation of target gene expression within 5-8 h following transduction. Here we have used the adenoviral delivery system combined with expression array analysis to identify novel putative PPARgamma target genes in murine fibroblasts and to determine the role of the A/B-domain in PPARgamma mediated transactivation of genomic target genes. Of the 257 genes found to be induced by PPARgamma2 expression, only 25 displayed A/B-domain dependency, i.e. significantly reduced induction in the cells expressing the truncated PPARgamma lacking the A/B-domain (PPARgammaCDE). Nine of the 25 A/B-domain dependent genes were involved in lipid storage and in line with this, triglyceride accumulation was considerably decreased in the cells expressing PPARgammaCDE compared to cells expressing full length PPARgamma2. Using chromatin immunoprecipitation (ChIP) we demonstrate that PPARgamma binding to genomic target sites and recruitment of the mediator component TRAP220/MED1/PBP/DRIP205 is not affected by the deletion of the A/B-domain. By contrast, the PPARgamma-mediated CBP and p300 recruitment to A/B-domain dependent target genes is abolished by deletion of the A/B-domain. These results indicate that the A/B-domain of PPARgamma2 is specifically involved in the recruitment or stabilization of CBP and p300 containing co-factor complexes to a subset of target genes.
Publication Title
No associated publication
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 5 Downloadable Samples
Description
The ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am
Publication Title
Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
Description
Lactobacilli are probiotics that, among other health promoting effects, have been ascribed immunostimulating and virus preventive properties. Certain lactobacilli species have been shown to possess strong IL-12 inducing properties. As IL-12 production depends on the up-regulation of type I interferons, we hypothesized that the strong IL-12 inducing capacity of L. acidophilus NCFM in murine bone marrow derived DC is caused by an up-regulation of IFN-, which subsequently stimulates the induction of IL-12 and the dsRNA binding toll like receptor (TLR)-3. The expression of the genes encoding IFN-, IL-12, IL-10 and TLR-3 in DC upon stimulation with L. acidophilus NCFM was measured. L. acidophilus NCFM induced a much stronger expression of ifn-, il-12 and il-10 compared to the synthetic dsRNA ligand Poly I:C, whereas the levels of expressed tlr-3 were similar. By the use of whole genome microarray gene expression, we investigated whether other genes related to the viral defence were up-regulated in DC upon stimulation with L. acidophilus NCFM and found that various virus defence related genes, both early and late, were among the strongest up-regulated genes. The IFN- stimulating capability was also detected in another L. acidophilus strain, but was not a property of other probiotic bacteria tested (B. bifidum and E. coli nissle).The IFN- inducing capacity was markedly reduced in TLR-2 -/- DCs, dependent on endocytosis and the major cause of the induction of il-12 and tlr-3 in L. acidophilus NCFM stimulated cells. Collectively, our results reveal that certain lactobacilli trigger the expression of viral defence genes in DC in a TLR-2 manner through induction of IFN- .
Publication Title
Lactobacillus acidophilus induces virus immune defence genes in murine dendritic cells by a Toll-like receptor-2-dependent mechanism.
Sample Metadata Fields
Treatment, Time
View Samples- Mus musculus
- 101 Downloadable Samples
Description
Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 60 Downloadable Samples
Description
Congenital malformations in facial bones significantly impact the overall representation of face. Establishing a correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investiation we will generate gene expression profile of different facial bones at different time intrevals over a period of 5 years to establish their roles in regulating craniofacial development
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples
GSE13880- Mus musculus, Homo sapiens
- 8 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 11 Downloadable Samples
Description
We investigated Smad4-mediated TGF-beta signaling in the development of occipital somite-derived myogenic progenitors during tongue morphogenesis by comparing the transcriptomes of tongue derived from Myf5-Cre;Smad4flox/flox mutant and Myf5-Cre;Smad4flox/+ control mice at day E13.5. Based on gene expression profiles and functional studies, we elucidated the influences Smad4 activity and TGF-beta signaling have on the gene expression profiles underlying tongue development. The data are consistent with the hypothesis that TGF-beta-Smad4-FGF6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression during tongue myogenesis.
Publication Title
A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Description
To elucidate the mechanism of BCL6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed BCL6+/+ and BCL6-/- B cell precursors. Pharmacological inhibition of BCR-ABL1 was performed with the BCR-ABL1 kinase inhibitor STI571 (Imatinib).
Publication Title
BCL6 is critical for the development of a diverse primary B cell repertoire.
Sample Metadata Fields
Sex, Age, Specimen part, Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
Description
To identify differences in the gene regulation between BCL6+/+ and BCL6-/- CML cells a gene expression analysis has been performed. We investigated the gene expression pattern in BCL6+/+ cells in the presence or absence of Imatinib and a combination of Imatinib and RI-BPI (a novel retro-inverso BCL6 peptide inhibitor). In BCL6-/- CML cells, we investigated the gene expression pattern in the presence or absence of Imatinib.
Publication Title
No associated publication
Sample Metadata Fields
Age, Disease, Disease stage
View Samples